Abstract
Summary There is demonstrable in rabbits an active, non-type-specific immunity against intrapleural infection with a highly virulent strain of Pneumococcus Type 1. This immunity may be produced by prolonged immunization with rough Pneumococcus Type 2. This non-type-specific immunity could not be passively transferred to normal rabbits. However, the immunity could be passively transferred by serum to other rabbits if the site of infection (pleural cavity) were already the site of a 72-hour aleuronat-starch inflammation. This active immunity seems to depend on the ability of the tissues of the immunized animal to dispose of the injected organisms promptly. While neither blood nor serum from actively immunized animals would kill virulent pneumococci, the pleural exudate from rough Pneumococcus 2 immune rabbits was markedly bactericidal for virulent Type 1 pneumococcus. Exudate from animals immunized with virulent Type 1 organisms was not bactericidal to a significantly larger degree. Normal exudate was not bactericidal. Minced splenic tissue from animals immunized with rough Pneumococcus Type 2 was bactericidal for large numbers of virulent Type 1 pneumococci. Normal splenic tissue was only feebly bactericidal. Cells obtained from immunized animals, when transferred to normal animals, would not protect against infection with Pneumococcus 1, whereas normal rabbit-cells, resuspended in supernate from the pleural exudate of Pneumococcus 2 (rough) immune animals produced a high degree of protection against Pneumococcus 1. Immune supernate, when passively transferred, did not protect. Pleural exudates from immunized animals showed a higher percentage of macrophages than did normal exudates. These macrophages were more highly phagocytic than the macrophages of normal exudate; however, this increased phagocytic power was non-specific. The antiserum produced by immunization with rough Type 2 pneumococcus had no opsonic effect on the highly virulent Pneumococcus Type 1 used for infection. The protective value of species-specific antiserum could not be related either to the “C” polysaccharide antibody or to heterophile antibody present in rough pneumococcal antiserum. The possible manner in which species-specific antibody exerts its protective power is discussed.
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